Mutants of glucokinase cause hypoglycaemia- and hyperglycaemia syndromes and their analysis illuminates fundamental quantitative concepts of glucose homeostasis.
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Effects of novel maturity-onset diabetes of the young (MODY)-associated mutations on glucokinase activity and protein stabilityMolecular physiology of mammalian glucokinaseHomotropic allosteric regulation in monomeric mammalian glucokinasePresent status of clinical deployment of glucokinase activatorsInsights into the pathogenicity of rare missense GCK variants from the identification and functional characterization of compound heterozygous and double mutations inherited in cisComputational modeling of glucose transport in pancreatic β-cells identifies metabolic thresholds and therapeutic targets in diabetesFunctional characterization of MODY2 mutations highlights the importance of the fine-tuning of glucokinase and its role in glucose sensingCharacterization of glucokinase regulatory protein-deficient miceComparative genetic analysis: the utility of mouse genetic systems for studying human monogenic disease.Lys169 of human glucokinase is a determinant for glucose phosphorylation: implication for the atomic mechanism of glucokinase catalysis.Structure-based predictive models for allosteric hot spots.Naturally occurring glucokinase mutations are associated with defects in posttranslational S-nitrosylation.Clinical heterogeneity in monogenic diabetes caused by mutations in the glucokinase gene (GCK-MODY).Opposite clinical phenotypes of glucokinase disease: Description of a novel activating mutation and contiguous inactivating mutations in human glucokinase (GCK) gene.A phospho-BAD BH3 helix activates glucokinase by a mechanism distinct from that of allosteric activatorsAnalysis of the co-operative interaction between the allosterically regulated proteins GK and GKRP using tryptophan fluorescenceIdentification and functional characterisation of novel glucokinase mutations causing maturity-onset diabetes of the young in Slovakia.Thermal stability of glucokinase (GK) as influenced by the substrate glucose, an allosteric glucokinase activator drug (GKA) and the osmolytes glycerol and ureaGlucokinase (GCK) mutations and their characterization in MODY2 children of southern Italy.Order-disorder transitions govern kinetic cooperativity and allostery of monomeric human glucokinasePhenotypic severity of homozygous GCK mutations causing neonatal or childhood-onset diabetes is primarily mediated through effects on protein stability.Bisphenol A impairs hepatic glucose sensing in C57BL/6 male mice.Glucagon-like peptide 1 stimulates post-translational activation of glucokinase in pancreatic beta cells.Discovery of a novel site regulating glucokinase activity following characterization of a new mutation causing hyperinsulinemic hypoglycemia in humansGene-altered mice and metabolic flux control.GCK-MODY (MODY 2) Caused by a Novel p.Phe330Ser Mutation.Glucokinase links Krüppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver diseaseAdenine nucleotide regulation in pancreatic beta-cells: modeling of ATP/ADP-Ca2+ interactions.Association with nitric oxide synthase on insulin secretory granules regulates glucokinase protein levels.GCK-MODY diabetes associated with protein misfolding, cellular self-association and degradation.Metabolite profiling reveals normal metabolic control in carriers of mutations in the glucokinase gene (MODY2)Evidence-based tailoring of bioinformatics approaches to optimize methods that predict the effects of nonsynonymous amino acid substitutions in glucokinase.When is it MODY? Challenges in the Interpretation of Sequence Variants in MODY Genes.Susceptibility of glucokinase-MODY mutants to inactivation by oxidative stress in pancreatic β-cells.Chronic treatment with a glucokinase activator delays the onset of hyperglycaemia and preserves beta cell mass in the Zucker diabetic fatty rat.GCK-MODY in the US National Monogenic Diabetes Registry: frequently misdiagnosed and unnecessarily treated.Glucokinase thermolability and hepatic regulatory protein binding are essential factors for predicting the blood glucose phenotype of missense mutations.Binding of ATP at the active site of human pancreatic glucokinase--nucleotide-induced conformational changes with possible implications for its kinetic cooperativity.Catalytic activation of human glucokinase by substrate binding: residue contacts involved in the binding of D-glucose to the super-open form and conformational transitions.Human pancreatic glucokinase (GlkB) complements the glucose signalling defect of Saccharomyces cerevisiae hxk2 mutants.
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P2860
Mutants of glucokinase cause hypoglycaemia- and hyperglycaemia syndromes and their analysis illuminates fundamental quantitative concepts of glucose homeostasis.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@en
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@nl
type
label
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@en
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@nl
prefLabel
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@en
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@nl
P2093
P356
P1433
P1476
Mutants of glucokinase cause h ...... ncepts of glucose homeostasis.
@en
P2093
Buettger C
Cuesta-Muñoz A
Matschinsky FM
P2888
P304
P356
10.1007/S001250051289
P577
1999-10-01T00:00:00Z